Bronchopulmonary Dysplasia and Ureaplasma: What Do We Know So Far?

Bronchopulmonary dysplasia (BPD) is the most common morbidity of prematurity. BPD is a chronic respiratory disease related to lung-injury during the primary course of critical lung disease such as respiratory distress syndrome or when abnormal development of the preterm lung occurs. Abnormal lung development not only results from primary lung injury in the first days after birth, but also secondary injury through abnormal repair resulting in arrested and abnormal alveolarization, fibrosis and pulmonary vascular dysgenesis. Chorioamnionitis is a risk factor that plays an important role in the development of BPD. Ureaplasma subspecies (spp.) are the most common isolated organisms from chorioamniotic tissue after premature births. Therefore Ureaplasma spp. appear to play an important role in the development of BPD, and treatment or prophylactic treatment of these infections or colonization may reduce the incidence, morbidity and mortality of BPD. Ureaplasma spp. infections are challenging not only to treat, but also to diagnosis in a timely manner. This review summarizes the current state of treatment and new developments in the treatment of Ureaplasma exposure in premature infants.

Patterns and etiology of acute and chronic lung injury: insights from experimental evidence / 中国当代儿科杂志

Adequate pulmonary function is pivotal for preterm infants. Besides being structurally immature, the preterm lung is susceptible to injury resulting from different prenatal conditions and postnatal insults. Lung injury might result in impaired postnatal lung development, contributing to chronic lung disease of prematurity, bronchopulmonary dysplasia (BPD). This review focuses on lung injury mediated by and related to inflammatory changes in the lung. We give an overview on experimental models which have helped to elucidate mechanisms of pulmonary inflammation in prematurity. We describe experimental data linking acute and chronic chorioamnionitis with intrapulmonary inflammation, lung maturation and surfactant production in various animal models. In addition, experimental data has shown that fetal inflammatory response is modulated by the fetus himself. Experimental data has therefore helped to understand differential effects on lung function and lung maturation exerted by maternal administration of potentially anti-inflammatory substances like glucocorticosteroids (GCS). New approaches of modulation of pulmonary inflammation/injury caused by postnatal interventions during resuscitation and mechanical ventilation have been studied in animal models. Postnatal therapeutic interventions with widely used drugs like oxygen, steroids, surfactant, caffeine and vitamin A have been experimentally and mechanistically assessed regarding their effect on pulmonary inflammation and lung injury. Carefully designed experiments will help to elucidate the complex interaction between lung injury, lung inflammation, repair and altered lung development, and will help to establish a link between lung alterations originating in this early period of life and long-term adverse respiratory effects.